Nitric oxide mediates iron-induced ferritin accumulation in Arabidopsis

Authors

  • Irene Murgia,

    Corresponding author
    1. Sezione di Fisiologia e Biochimica delle Piante, Dipartimento di Biologia, Università degli Studi di Milano, via Celoria 26, 20133 Milano, Italy, and
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  • Massimo Delledonne,

    1. Dipartimento Scientifico e Tecnologico, Università degli Studi di Verona, Strada Le Grazie 15 – Ca′ Vignal – 37134 Verona – Italy
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  • Carlo Soave

    1. Sezione di Fisiologia e Biochimica delle Piante, Dipartimento di Biologia, Università degli Studi di Milano, via Celoria 26, 20133 Milano, Italy, and
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For correspondence (fax +39 02 50314815; e-mail irene.murgia@unimi.it).

Summary

Nitric oxide (NO) is a signaling molecule that plays a critical role in the activation of innate immune and inflammatory responses in animals. During the last few years, NO has also been detected in several plant species and the increasing number of reports on its function in plants have implicated NO as an important effector of growth, development and defense. Analogously to animals, NO has been recently shown to inhibit tobacco aconitase. This suggests that NO may elevate free iron levels in the cells by converting tobacco cytoplasmic aconitase into a mRNA binding protein that negatively regulates accumulation of ferritin.

    We investigated the possible role of NO as a regulator of ferritin levels in Arabidopsis and found that the NO-donor sodium nitroprusside (SNP) induces accumulation of ferritin both at mRNA and protein level. Iron is not necessary for this NO-mediated ferritin transcript accumulation, since SNP is still able to induce the accumulation of ferritin transcript in Arabidopsis suspension cultures pre-treated with the iron chelants DFO or ferrozine. However, NO is required for iron-induced ferritin accumulation, as the NO scavenger CPTIO prevents ferritin transcript accumulation in Arabidopsis suspension cultures treated with iron. The pathway is ser/thr phosphatase-dependent and necessitates protein synthesis; furthermore, NO mediates ferritin regulation through the IDRS sequence of the Atfer1 promoter responsible for transcriptional repression under low iron supply.

    NO, by acting downstream of iron in the induction of ferritin transcript accumulation is therefore a key signaling molecule for regulation of iron homeostasis in plants.

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